AbnormalFHIT transcripts found in both lung cancer and normal lung tissue

1999 ◽  
Vol 24 (2) ◽  
pp. 105-111 ◽  
Author(s):  
Yoshio Tokuchi ◽  
Yasuhito Kobayashi ◽  
Shin-ichi Hayashi ◽  
Moriaki Hayashi ◽  
Keiji Tanimoto ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Lung Tissue ◽  
Normal Lung Tissue ◽  
Normal Lung

Micro-RNA signature differences in lung adenocarcinoma with specific driver alterations.

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. 11066-11066
Author(s):  
Lorenza Landi ◽  
Pierluigi Gasparini ◽  
Stefania Carasi ◽  
Carmelo Tibaldi ◽  
Luciano Cascione ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Lung Adenocarcinoma ◽  
Lung Tissue ◽  
Kras Mutation ◽  
Triple Negative ◽  
Egfr Mutation ◽  
Differential Expression Analysis ◽  
Normal Lung Tissue ◽  
Normal Lung ◽  
Expression Levels

11066 Background: Oncogenic driving alterations define types of lung adenocarcinoma with different prognosis and sensitivity to targeted agents. MicroRNAs (miRNAs) are a new class of non-coding RNAs involved in gene expression regulation. How miRNAs are dysregulated in lung cancer with ALK translocation, EGFR or KRAS mutation is unknown. In this study we aimed to identify miRNA signatures according to the presence of specific driver and to correlate miRNAs deregulation with patient outcome. Methods: The study was conducted in a cohort of 70 lung cancer patients (pts) including 18 ALK+ tumors, 11 ALK-/EGFR mutation+, 15 ALK-/KRAS mutation+, 26 ALK-/EGFR and KRAS wild-type and defined as triple negative. Matched normal lung tissue from 18 cases representative of the entire cohort were also included onto the analysis. RNA was isolated from formalin-fixed paraffin-embedded tissue (FFPE), using the Recover ALL kit (Ambion). NanoString nCounter system platform was used to generate the miRNA profile. We used Limma to test for differential expression analysis of data. The miR-515 family expression between tissues was validated by RT-qPCRs, analyzed using the parametric t-test (unpaired, 2-tailed for validation). Results: miRNA expression profile clusters distinctly ALK+ pts from ALK- and normal lung tissue. Within the ALK- group we found specific miRNAs subsets able to sub-stratify KRAS versus EGFR careers clustering sharply triple negative versus EGFR mutation+ and triple negative versus KRAS mutation+. miRNAs belonging to the miR-515 family seems to be the most deregulated in the ALK+ versus ALK-. Although their expression is stably high in normal tissues and ALK+ class, they are highly downregulated in KRAS mutated versus EGFR mutated and versus triple negative (p-value <0.001 for all comparisons). Conclusions: miRNAs profile significantly differs in pts with ALK translocation, EGFR mutations and KRAS mutations. Analysis of miR-515 family members is ongoing in order to correlate their expression levels with pts’ outcome. In vitro modulation of miR-515 family expression levels, together with drugs treatment are ongoing in order to find possible chemo-resistance/chemo-sensitivity miRNA dependent, in ALK+ and ALK- model.

scholarly journals OC-0375 Improving lung cancer outcome by reducing normal lung tissue toxicity

2019 ◽  
Vol 133 ◽  
pp. S186-S187
Author(s):  
L. Giuranno ◽  
E. Roig Moreno ◽  
R. Iannone ◽  
M. Vooijs
Keyword(s):  
Lung Cancer ◽  
Lung Tissue ◽  
Normal Lung Tissue ◽  
Normal Lung ◽  
Cancer Outcome

scholarly journals P1.02-009 Accumulation of Mutations in Background Normal Lung Tissue Constitutes a Major Lung Cancer Risk

2017 ◽  
Vol 12 (11) ◽  
pp. S1927-S1928
Author(s):  
E. Kubo ◽  
H. Takeshima ◽  
S. Yamashita ◽  
N. Motoi ◽  
T. Ushijima
Keyword(s):  
Lung Cancer ◽  
Cancer Risk ◽  
Lung Tissue ◽  
Lung Cancer Risk ◽  
Normal Lung Tissue ◽  
Normal Lung

Expression of BCRP gene in the normal lung tissue and lung cancer

2001 ◽  
Vol 13 (1) ◽  
pp. 22-26
Author(s):  
You-sheng Mao ◽  
Austin Doyle ◽  
Weidong Yang ◽  
Yuetong Wei ◽  
Mark J. Krasna ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Lung Tissue ◽  
Normal Lung Tissue ◽  
Normal Lung

scholarly journals Immunofluorescent analyses of tumor marker beta-III tubuilin expression in tumor and ajacent normal lung tissue derived from patients with non-small cell lung cancer

2016 ◽  
Vol 15 (2) ◽  
pp. 16-18 ◽  
Author(s):  
I. A. Mamichev ◽  
T. A. Bogush ◽  
E. A. Dudko ◽  
O. M. Ryabinina ◽  
A. N. Grishanina ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Lung Tissue ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Normal Lung Tissue ◽  
Normal Lung ◽  
Small Cell Lung ◽  
Biopsy Specimens ◽  
Tissue Specimens

Background. Class III beta-tubulin (TUBB3) is one of the eight beta tubulin isotypes identified in human. It is constitutively expressed in brain and testis but not in lung tissue. TUBB3 is also known to appear in solid tumors, in particular in non-small cell lung cancer (NSCLC), and it is often associated with poor prognosis and resistance to taxanes and Vinka alkaloids. Objective: We have suggested that TUBB3 expression may cover not only the primary tumor but also a wide adjacent area of morphologically normal lung tissue. To check the hypothesis we have measured TUBB3 expression both in the non-small cell lung carcinoma (NSCLC) and remote lung tissue derived from the same lung. 60surgical biopsy specimens of NSCLC and morphologically normal lung tissue of 30patients were investigated. Materials and methods. Biopsy specimens were converted to suspension, fixed in 4 % formaldehyde and analyzed by flow cytometry using monoclonal antibodies to TUBB3. The method was developed in the laboratory of medicinal chemistry research Institute of experimental diagnostics and therapy of tumors (N.N. Blokhin Russian Cancer Research Center) and patented. Results. Fraction of TUBB3-positive cells in the group of adjacent lung tissue specimens was lower compared to NSCLC group but still positive in the majority of adjacent lung tissue specimens (25 of 30) and achieved up to 39 % of cells. Conclusion. We suggest that TUBB3 expression in adjacent morphologically normal lung tissue indicates presence of transformed and potentially malignant cells far from the primary site.

scholarly journals Intratumoural heterogeneity and immune modulation in lung adenocarcinoma of female smokers and never smokers

2021 ◽  
Author(s):  
Timo Benedikt Trefzer ◽  
Marc A. Schneider ◽  
Katharina Jechow ◽  
Lorenz Robert Chua ◽  
Thomas Muley ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Lung Adenocarcinoma ◽  
Lung Tissue ◽  
Significant Proportion ◽  
Cellular Heterogeneity ◽  
Tobacco Smoke Exposure ◽  
Smoking History ◽  
Normal Lung Tissue ◽  
Normal Lung ◽  
Never Smokers

Lung cancer is still the leading cause of cancer death worldwide despite declining smoking prevalence in industrialised countries. Although lung cancer is highly associated with smoking status, a significant proportion of lung cancer cases develop in patients who never smoked, with an observable bias towards female never smokers. A better understanding of lung cancer heterogeneity and immune system involvement during tumour evolution and progression in never smokers is therefore highly warranted. We employed single nucleus transcriptomics of surgical lung adenocarcinoma (LADC) and normal lung tissue samples from patients with or without smoking history. Immune cells as well as fibroblasts and endothelial cells respond to tobacco smoke exposure by inducing a highly inflammatory state in normal lung tissue. In the presence of LADC, we identified differentially expressed transcriptional programmes in macrophages and cancer-associated fibroblasts, providing insight into how the niche favours tumour progression. Within tumours, we distinguished eight subpopulations of neoplastic cells in female smokers and never smokers. Through pseudotemporal ordering, we inferred a trajectory towards two differentiated tumour cell states implicated in cancer progression and invasiveness. A proliferating cell population sustaining tumour growth exhibits differential immune modulating signatures in both patient groups. Our results resolve cellular heterogeneity and immune interactions in LADC, with a special emphasis on female never smokers and implications for the design of therapeutic approaches.

Microsatellite alteration in histologically normal lung tissue of patients with non-small cell lung cancer

Lung Cancer ◽  
2000 ◽  
Vol 30 (2) ◽  
pp. 83-89 ◽  
Author(s):  
Jae Yong Park ◽  
Hyo-Sung Jeon ◽  
Sun Ha Park ◽  
Tae In Park ◽  
Ji-Woong Son ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Lung Tissue ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Normal Lung Tissue ◽  
Normal Lung ◽  
Small Cell Lung

scholarly journals Phospholipid dynamics in ex vivo lung cancer and normal lung explants

2021 ◽  
Author(s):  
Julia Lesko ◽  
Alexander Triebl ◽  
Elvira Stacher-Priehse ◽  
Nicole Fink-Neuböck ◽  
Jörg Lindenmann ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Lung Tissue ◽  
De Novo ◽  
Ex Vivo ◽  
Normal Lung Tissue ◽  
Normal Lung ◽  
Cancer Tissue ◽  
Glycerol Backbone ◽  
Lung Cancer Tissue

AbstractIn cancer cells, metabolic pathways are reprogrammed to promote cell proliferation and growth. While the rewiring of central biosynthetic pathways is being extensively studied, the dynamics of phospholipids in cancer cells are still poorly understood. In our study, we sought to evaluate de novo biosynthesis of glycerophospholipids (GPLs) in ex vivo lung cancer explants and corresponding normal lung tissue from six patients by utilizing a stable isotopic labeling approach. Incorporation of fully 13C-labeled glucose into the backbone of phosphatidylethanolamine (PE), phosphatidylcholine (PC), and phosphatidylinositol (PI) was analyzed by liquid chromatography/mass spectrometry. Lung cancer tissue showed significantly elevated isotopic enrichment within the glycerol backbone of PE, normalized to its incorporation into PI, compared to that in normal lung tissue; however, the size of the PE pool normalized to the size of the PI pool was smaller in tumor tissue. These findings indicate enhanced PE turnover in lung cancer tissue. Elevated biosynthesis of PE in lung cancer tissue was supported by enhanced expression of the PE biosynthesis genes ETNK2 and EPT1 and decreased expression of the PC and PI biosynthesis genes CHPT1 and CDS2, respectively, in different subtypes of lung cancer in publicly available datasets. Our study demonstrates that incorporation of glucose-derived carbons into the glycerol backbone of GPLs can be monitored to study phospholipid dynamics in tumor explants and shows that PE turnover is elevated in lung cancer tissue compared to normal lung tissue.

Sign in / Sign up

Export Citation Format

Share Document